Infectious pneumonia is one of the most common complications after bone marrow transplantation (BMT), which is considered to be associated with poor reconstitution and functional maturation of alveolar macrophages (AMs) post-transplantation. Here, we present evidence showing that lack of IL-13-secreting group 2 innate lymphoid cells (ILC2s) in the lungs may underlay poor AM reconstitution in a mouse model of haploidentical BMT (haplo-BMT). Recombinant murine IL-13 was able to potentiate monocyte-derived AM differentiation in vitro. When intranasally administered, a cocktail of granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-13, and CCL2 not only promoted donor monocyte-derived AM reconstitution in haplo-BMT-recipient mice but also enhanced the innate immunity of the recipient animals against pulmonary bacterial infection. These results provide a useful clue for a clinical strategy to prevent pulmonary bacterial infection at the early stage of recipients post-BMT.

感染性肺炎是骨髓移植（BMT）后最常见的并发症之一，被认为与移植后肺泡巨噬细胞（AMs）重建不良和功能成熟有关。在这里，我们提供的证据表明，在半相合 BMT (haplo-BMT) 小鼠模型中，肺中缺乏分泌 IL-13 的第 2 组先天淋巴细胞 (ILC2) 可能是 AM 重建不良的基础。重组鼠 IL-13 能够增强单核细胞衍生的 AM 分化体外. 鼻内给药时，粒细胞-巨噬细胞集落刺激因子 (GM-CSF)、IL-13 和 CCL2 的混合物不仅促进了单倍体 BMT 受体小鼠的供体单核细胞来源的 AM 重建，而且增强了小鼠的先天免疫。受体动物抵抗肺部细菌感染。这些结果为在接受 BMT 后早期预防肺部细菌感染的临床策略提供了有用的线索。